The hypothesis behind the protocol entitled "Leukotriene B4 and Glucocorticoid Insensitive Asthma" is that the upregulation of 5 lipoxygenase and leukotriene B4 production by glucocorticoids (GC) leads to an influx and activation of neutrophils into the airways of certain asthmatic patients which limits their responses to GC. We have observed that glucocorticoid insensitive asthmatics (GIA) develop a neutrophilic influx following treatment with prednisone (40 mg/day x 7 days), which is associated with an increase in bronchoalveolar lavage LTB4 levels. The aims of the study are to determine whether the monocyte/macrophage and/or the neutrophil are the source for the LTB4 and whether this upregulation is modulated by an effect through GM-CSF or IL-13 on enzymes in the 5 lipoxygenase pathway. At the present time, it appears that both monocytes and neutrophils increase LTB4 production after GC in GIA. The mechanisms behind that upregulation remain to be elucidated.